Cardiovascular Disease Congestive Heart Failure; Transplant, Pacemakers Congestive Heart Failure (CHF) Definition: Inabilility of the heart to deliver oxygenated blood to metabolizing tissues, secondary to impairment in Q, depressed LV systolic function, diastolic function, abnormalities in skeletal muscle metabolism or pulmonary function, or combinations, thereof (ACSM, 2000, pg 186) CHF: Pathophysiology (Brubaker, pg 7, 1999) Decreased Q Pulmonary mismatching CHF: Pressure-volume (performance) curve Increased contractility Systolic and/or Diastolic dysfunction Myocardial disease Increased afterload Increased preload Neurohormonal activation Vasoconstriction Activation of Frank-Starling mechanism Stroke volum me (or Q) hypertension Normal Heart failure Pulmonary congestion LV End-diastolic pressure (or end-diastolic volume) Presentation CHF: LV Dysfunction? < 65 yr >65 yr Progressive SOB Acute SOB CHF: LV Ventricular Characteristics End-diastolic Dysfunction (ml) End-systolic Dysfunction (ml) Stroke volume (ml) Ejection fraction (%) Physical exam Radiograph ECG Displaced PMI S3 gallop Pulmonary congestion Cardiomegaly Q waves Sustained PMI S4 gallop pulmonary congestion Normal heart size LV hypertrophy Normals Systolic dysfunction Diastolic dysfunction 120 55 65 55 160 110 50 30 85 35 50 60 Echo Decreased EF Normal or increased EF Ehrman JK, et al. Clinical Exercise Physiology. Table 15.1, pg 263 1
CHF: Signs and symptoms Exercise intolerance Peripheral edema Paroxysmal nocturnal dyspnea Dyspnea on exertion Orthopnea CHF: Medical Management Need to identify the underlying cause Pharmacologic Reduce volume overload diuretics Reduce afterload ACE inhibitor Shift blood volume - nitroglycerin/prusside Improve inotropic function - digoxin Transplant last resort Low EF, with high chance of survival CHF: Exercise Responses Acute Reduced Q relative to work demand Shortness of breath Blunted systolic blood pressure response Early leg fatigue Training Historical perspective (before/after the 80s) Improve Q due to peripheral adaptations Exercise training in those with less than 40% EF is controversial (Table 15.4, pg 271) See Table 15.3, pg 269 in CEP text CHF: Exercise Testing Low level incremental tests with ~ 1 MET increases per stage (5 MET pk capacity) Naughton or ramp 6 minute walk test Often exertional hypotension, dysrhythmias, h and chronotropic incompetence Needs to be a symptom limited test Value of gas exchange Extremely helpful for risk stratification Weber classification Other Echocardiography Dx use for LV function CHF: Exercise prescription Aerobic Intensity Borg 11-16 40 to 75% VO2 pk or HR reserve Frequency 3 7 days per week Duration 20 40 minutes per session Strength circuit training Flexibility 2 3 days (ROM) Cardiac Transplant End-stage CHF Performed on ~ 3,000 4,000 pts/yr Exercise training is important after surgery for improved quality of life and clinical outcomes Denervation is the main issue as well as side effects of immunosuppressive drugs 2
Exercise Responses Drastically reduced functional capacity Heart rate Elevated resting and exercise after surgery Blunted heart rate response to exercise May see higher BPs due to immunosuppressive medications Cardiac Transplant: Exercise Testing/Programming Phase I First SL-GXT is performed about 4 to 6 weeks after surgery. Usually on treadmill, but may be completed on cycle ergometer. Most likely need to avoid arm ergometry until patient is completed healed from the surgery Cardiac Transplant: Exercise Programming (see also PA 15.5) Phase II and III 3to5daysperweekfor30to60minutes 30 of aerobic exercise Target RPE 60 to 70% of max METs Case study 15 Peripheral Arterial Disease (PAD) Affects 12% of general population and 20% of older adults Pathophysiology mismatch between supply and demand to muscle which leads to Deconditioning Denervation Impaired oxidative metabolism Claudication PVD: Pathophysiology May affect arteries (PAD), veins, or lymphatic system PAD is due to one or more of the following Structural changes in the vessel wall Narrowing of the vascular lumen Spasm of vascular smooth muscle Major classes of PVD Aortic Arterial = PAD Veins PAD From Lilly, pg 311, 1998 3
PAD: Evaluation ABI and Exercise (CEP Text) WIQ walking impairment questionnaire Assessment/Screening Graded Exercise Test, followed by post-exercise evaluation of the ratio for arterial blood flow in the upper limb (arm) and the lower limb (ankle). Low ratios indicate perfusion deficits and thresholds allow classifications of disease severity. The flow deficit can be quantified using ABI (Ankle Brachial Index). Patients with abnormal ABI might be re-evaluated at 2 month intervals following use of interventions such as exercise. Gait analysis PAD: Medical Management (see table 17.3, CEP text) Improve claudication pain and reduce risk factors Common Medications Pentoxifylline Dipyridamole Warfarin Aspirin Little information about the interaction of medications and exercise training Angioplasty and surgery PAD: Exercise Testing Claudication-free walking time or distance (ICD) Maximal, claudication-limited walking time or distance (ACD) Some use constant load tests (6 minute test) Incremental treadmill 3 min stages, 2 mph, 3.5% grade increases 3 min stages, 2 mph, 2% grade increases May also have to consider arm ergometer PAD Exercise Testing and Training: Severity Rating Grade 0 = asymptomatic Grade 1 = intermittent claudication Grade 2 = ischemic rest pain Grade 3 = minor or major tissue loss from the foot PAD: Exercise Prescription Aerobic Exercise - perform activity at 40% of VO 2 pk, until the patient reaches 3-4 on the standard PVD pain scale. Objective is to reach 75% for 40 minutes Resistance Exercise - perform each exercise at 80% of 1RM for 6-8 movements, continue free breathing with each movement; alternate exercises for specific areas of body to promote recovery in different muscle groups 4
PAD: Mechanisms of Improvement Peripheral Blood Flow Discrepancy in literature for blood flow May find decreased blood viscosity, increased capillary density Muscle Metabolism Reduces the plasma concentration of short-chain acylcarnitines which may improve aerobic muscle metabolism Pacemakers Figure 18.2 Dual Pacer Pre-disposing conditions (Table 18.1) A-V block Sick sinus syndrome w/ symptomatic bradycardia Uncontrolled symptomatic atrial-fibrillation, survivors of sudden cardiac death Types Based on Standardized code I.e. VVIR Implantable Cardioverter Defibrillators Single-chamber pacemaker Dual-chamber pacemaker Figure 18.1 Demand Pacer Pacemakers: Exercise responses Acute Primarily abnormal heart rate responses May receive inappropriate defibrillation (ICD) Training Important that exercise threshold be below ischemic threshold and below defibrillation threshold 5
Exercise Responses - Figure 18.4 Pacemakers: Exercise Testing Establishing lower and upper rate limits Evaluation Treadmill 1-2 METs per stage (2-3 minute stages) Peak heart rate may be blunted Cycle 10-25 watts per stage (2-3 min stages) Chronotropic Assessment Exercise Protocol Pacemakers: Prescription Prescription NOTE THE TYPE!!! 40 to 85% of pk heart rate reserve Keep pprescription p below ischemic and ICD threshold 4-7 days/wk 20 60 minutes session Circuit weight training O.K. several weeks after implantation Modified Karvonen TSBP = (SBP max SBP rest )(50-80%) + SBP rest Case Study 18 Resources used for this lecture American College of Sports Medicine. Exercise Management for Persons with Chronic Diseases and Disabilities. ed. J.L. Durstine. Champaign, Human Kinetics. American College of Sports Medicine. Resource Manual for Guidelines for Exercise Testing and Prescription. 4 th ed. Williams and Wilkins, 2001. American College of Sports Medicine. Guidelines for Exercise Testing and Prescription. 6 th ed. Lea & Febiger, 2000 Brubaker, P.H. Clinical consideration and exercise responses of patients with primary left ventricular diastolic dysfunction.clinical Exercise Physiology. 1(1). 1999, 5-12. Keteyian, S.J., Brawner, C.A., and Schairer, J.R. Exercise Testing and Training of Paitents with Heart Failure due to left vetricular systolic dysfunction. J. Cardiopulmonary Rehab. 17, 1997, 19-28. Lilly, L.S. ed. Pathophysiology of Heart Disease. 2 nd ed. Baltimore. Williams and Wilkins, 1998 Pollock, M.L. and Schmidt, D.H. ed. Heart Disease and Rehabilitation. 3 rd ed. Human Kinetics, 1995 6